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Releasing the Brake on Synaptic Plasticity: Immune Genes Moonlighting in Neurons
(
12/14/2011
)
63
minutes
Conference:
M.I.N.D. Institute Lecture Series on Neurodevelopmental Disorders
Host:
UC Davis MIND Institute
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description:
Connections in the adult visual system are highly precise, but they do not start out that way. Precision emerges during critical periods of development as synaptic connections remodel, a process requiring neural activity and involving regression of some synapses and strengthening and stabilization of others. We discovered, unexpectedly, that MHC Class I genes and an innate immune receptor, PirB, are involved in this process. Thus, MHCI ligands signaling via PirB receptor may function to "brake" activity- dependent synaptic plasticity. Together, results imply that these molecules, thought previously to function only in the immune system, also act at neuronal synapses to limit how much- or perhaps how rapidly- synapse strength changes in response to new experience. Changes in the function of these molecules may also contribute to developmental disorders such as autism and schizophrenia.
more on this subject:
The MET Receptor Tyrosine Kinase and Autism Risk
FGF Signaling and Neocortical Patterning
Automatically Mapping the Language Learning Environment of Young Children with Autism: Implications for Assessment and Intervention
see all from Neuroscience and Neurobiology >
conference links:
Lecture series information
more from this conference:
The MET Receptor Tyrosine Kinase and Autism Risk
FGF Signaling and Neocortical Patterning
Automatically Mapping the Language Learning Environment of Young Children with Autism: Implications for Assessment and Intervention
Neural Signatures of Atypical Brain Development in Autism
see all from this conference >